5 results match your criteria: "Academic Hospital Maastricht and Maastricht University[Affiliation]"

Increased release of sMD-2 during human endotoxemia and sepsis: a role for endothelial cells.

Mol Immunol

June 2008

Department of Surgery, Nutrition and Toxicology Research Institute Maastricht, Academic Hospital Maastricht and Maastricht University, Universiteitssingel 50, 6200 MD Maastricht, The Netherlands.

MD-2 is the crucial cofactor of TLR4 in the detection of LPS. Here, we show that soluble MD-2 (sMD-2) circulates in plasma of healthy individuals as a polymeric protein. The total amount of sMD-2 in septic plasma was strongly elevated and contained both sMD-2 polymers and monomers, the latter representing the putative biologically active form of MD-2.

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Serial left-ventricular biopsy sampling using a minimally invasive trans-thoracic approach in adult dogs.

Pflugers Arch

September 2007

Department of Cardiology, Cardiovascular Research Institute Maastricht, Academic Hospital Maastricht and Maastricht University, P.O. Box 5800, 6202 AZ, Maastricht, The Netherlands.

Myocardial biopsies are an increasingly important tool to unravel the molecular mechanisms of cardiac disease. We evaluate a novel minimally invasive trans-thoracic approach for left-ventricular (LV) intra-mural biopsies, which enables repetitive individual sampling in adult dogs. Forty three generally anaesthesised dogs were studied during sinus rhythm (SR, control) and multiple times after the induction of volume overload hypertrophy (complete atrioventricular block [AVB]).

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Redox-active iron, catalyzing the generation of reactive oxygen species, has been implicated in experimental renal ischemia-reperfusion injury. However, in clinical transplantation, it is unknown whether redox-active iron is involved in the pathophysiology of ischemic injury of non-heart-beating (NHB) donor kidneys. We measured redox-active iron concentrations in perfusate samples of 231 deceased donor kidneys that were preserved by machine pulsatile perfusion at our institution between May 1998 and November 2002 using the bleomycin detectable iron assay.

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Exogenous alpha-1-acid glycoprotein protects against renal ischemia-reperfusion injury by inhibition of inflammation and apoptosis.

Transplantation

October 2004

Department of Surgery, Nutrition and Toxicology Research Institute Maastricht (NUTRIM), Academic Hospital Maastricht and Maastricht University, Universiteitssingel 50, 6200 MD Maastricht, the Netherlands.

Background: Although ischemia-reperfusion (I/R) injury represents a major problem in posttransplant organ failure, effective treatment is not available. The acute phase protein alpha-1-acid glycoprotein (AGP) has been shown to be protective against experimental I/R injury. The effects of AGP are thought to be mediated by fucose groups expressed on the AGP protein inhibiting neutrophil infiltration.

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One of the first steps in the pathogenesis of endometriosis is the attachment of the endometrium to the peritoneal lining. Since the peritoneum is extremely fragile and hard to obtain, amnion has been used as an in-vitro model to study adhesion. Scanning and transmission electron microscopy was applied to evaluate the adhesion of endometrial cells isolated in the proliferative and secretory phases of the menstrual cycle.

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